Type
Text
Type
Thesis
Advisor
Marchenko, Natalia D | Cao, Jian.
Date
2014-12-01
Keywords
breast cancer, HER2, HSF1, mutp53 | Biochemistry
Department
Department of Biochemistry and Cell Biology.
Language
en_US
Source
This work is sponsored by the Stony Brook University Graduate School in compliance with the requirements for completion of degree.
Identifier
http://hdl.handle.net/11401/76928
Publisher
The Graduate School, Stony Brook University: Stony Brook, NY.
Format
application/pdf
Abstract
Breast cancer is the second deadliest cancer in the United States and is classified into four main subtypes including HER2-positive breast cancer. There have been a number of HER2-targeted therapeutic treatments that were discovered, but they are expensive and patients frequently exhibit a resistance for these treatments. To alleviate patients undergoing expensive therapy with the possibility of not benefitting from the treatment, it is important to understand the cooperation between HER2 and mutp53, a tumor suppressor gene that is mutated in the majority of breast cancers. Analysis of scientific articles illustrate that HER2 and mutp53 cooperate to promote tumorigenesis via the master transcriptional regulator of the heat shock response, HSF1 in HER2-positive breast cancer. Therefore, this HSFS1-mediated oncogenic cooperation between mutp53 and HER2 may amplify HER2 signaling and sensitize breast cancer cells to HER2 targeted therapies. Thus, mutp53 can be used as a potential biomarker for successful treatment of HER2-positive breast cancer. | 46 pages
Recommended Citation
Russo, Amanda Deanna, "Analysis of the oncogenic cooperation between mutp53 and HER2 to propose mutp53 as a biomarker for HER2-positive breast cancer" (2014). Stony Brook Theses and Dissertations Collection, 2006-2020 (closed to submissions). 2801.
https://commons.library.stonybrook.edu/stony-brook-theses-and-dissertations-collection/2801